Stubbs Sharron A, Hardy Kate, Da Silva-Buttkus Patricia, Stark Jaroslav, Webber Lisa J, Flanagan Adrienne M, Themmen Axel P N, Visser Jenny A, Groome Nigel P, Franks Stephen
Institute of Reproductive and Developmental Biology, Wolfson and Weston Research Centre for Family Health, Imperial College London, Hammersmith Hospital, London W12 0NN, United Kingdom.
J Clin Endocrinol Metab. 2005 Oct;90(10):5536-43. doi: 10.1210/jc.2005-0907. Epub 2005 Jul 19.
Polycystic ovary syndrome, the most common cause of anovulatory infertility, is characterized by disordered folliculogenesis, notably increased progression from the primordial to the primary stages. This ovarian phenotype is similar to that observed in mice lacking anti-müllerian hormone (AMH).
The objective of this study is to investigate whether AMH is involved in accelerating the transition of follicles from primordial to primary stages in polycystic ovaries.
This study compares AMH expression in archive tissue from normal and polycystic ovaries.
This is a laboratory-based study.
Ovarian tissue from seven normoovulatory women and 16 women with polycystic ovaries (five of whom were anovulatory) was used in this study. Ovaries were classified by histology and with reference to menstrual cycle history and ultrasound.
Presence and intensity of AMH expression in 1403 follicles was the main outcome measure.
AMH was observed from the primordial stage onward. AMH immunostaining was observed in significantly fewer primordial (P = 0.007) and transitional follicles (P = 0.001) in ovaries from anovulatory women with polycystic ovaries compared with women with regular cycles and either normal or polycystic ovaries. AMH-negative follicles had fewer pregranulosa cells in the largest cross-section of the follicle at both the primordial (median, four and six for AMH-negative and -positive follicles, respectively; P < 0.0001) and transitional stages (median six and nine; P < 0.0007) in normal tissue, and fewer at the transitional stage (median, seven and 11; P < 0.0001) in tissue from anovulatory women with polycystic ovaries. This suggests that AMH expression is associated with granulosa cell mitosis.
These findings indicate a relative deficiency of AMH in primordial and transitional follicles in ovaries from anovulatory women with polycystic ovaries. This may contribute to disordered early follicle development in polycystic ovary syndrome.
多囊卵巢综合征是无排卵性不孕最常见的原因，其特征为卵泡发生紊乱，尤其是从原始卵泡到初级卵泡阶段的进展显著增加。这种卵巢表型与在缺乏抗苗勒管激素（AMH）的小鼠中观察到的表型相似。
本研究的目的是调查AMH是否参与加速多囊卵巢中卵泡从原始阶段向初级阶段的转变。
本研究比较了正常卵巢和多囊卵巢存档组织中AMH的表达情况。
这是一项基于实验室的研究。
本研究使用了7名排卵正常女性和16名多囊卵巢女性（其中5名无排卵）的卵巢组织。卵巢通过组织学分类，并参考月经周期史和超声检查结果。
1403个卵泡中AMH表达的存在情况和强度是主要观察指标。
从原始卵泡阶段开始就观察到AMH。与月经周期正常的女性（无论卵巢正常与否）相比，多囊卵巢无排卵女性卵巢中的原始卵泡（P = 0.007）和过渡卵泡（P = 0.001）中观察到的AMH免疫染色明显较少。在正常组织中，AMH阴性卵泡在原始阶段（AMH阴性和阳性卵泡的最大横截面积中颗粒前体细胞的中位数分别为4个和6个；P < 0.0001）和过渡阶段（中位数为6个和9个；P < 0.0007）的颗粒前体细胞较少，而在多囊卵巢无排卵女性的组织中，过渡阶段（中位数为7个和11个；P < 0.0001）的颗粒前体细胞较少。这表明AMH表达与颗粒细胞有丝分裂有关。
这些发现表明，多囊卵巢无排卵女性卵巢中的原始卵泡和过渡卵泡中AMH相对缺乏。这可能导致多囊卵巢综合征早期卵泡发育紊乱。
